Fig. 1

The predicted influence of NER sub-pathways on the coding or template damaged strand of an actively transcribed gene. a and b Schematic representation of the repair of a bulky lesion located on the template strand (panel a) or on the coding strand (panel b) of an active gene. If the lesion is on the template strand (panel a), read by RNAPII during the transcription process, the lesion causes the RNAPII complex to stall. CSA and CSB proteins are the sensors of stalled RNAPII and recruit the transcription complex TFIIH to the site of the lesion. The helicase activities, XPB and XPD, of the TFIIH complex open the chromatin around the lesion. XPA and RPA stabilized the open structure of the chromatin. The endonucleases, ERCC1-XPF in 5′ and XPG in 3′ cleave the damaged strand. The gap is then filled by DNA repair polymerases and ligases. If the lesion is on the coding strand (panel b) and therefore not read by the RNAPII complex, the lesion does not interfere with the enzyme processivity and the gene is transcribed. The lesion can be later recognized by the XPC complex, the lesion binding proteins in the global genome repair (GGR), the second NER sub-pathway. After the lesion recognition step, both GGR and TCR are identical. In bold are the factors controlled for their impact on L1 insertion regulation in the present study